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CiteHealth » Home Care Agencies » Florida » Cities » Miami
Miami, Florida Home Care Agencies
Choose a Miami, Florida home care agency below to view a detailed report including information on services, quality, patient reviews, ratings, and more.
Showing providers 1 to 181 of 181
1st Class Home Health, Inc
1st Class Home Health, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
Based Upon 0 User Reviews
8660 W Flager Street #121
AA Advanced Care, Inc
AA Advanced Care, Inc was certified by Medicare in 2005 and is operated as a for-profit provider.
8700 W Flagler Street Suite 270
AAA Home Health Services, Inc
AAA Home Health Services, Inc was certified by Medicare in 2003 and is operated as a for-profit provider.
2929 Southwest 3rd Avenue Suite 520
ABC Home Healthcare, Inc
ABC Home Healthcare, Inc was certified by Medicare in 2005 and is operated as a for-profit provider.
ACE Home Health Services Corporation
ACE Home Health Services Corporation was certified by Medicare in 2006 and is operated as a for-profit provider.
10380 West Flagler Street
Advance Home Care, Inc
Advance Home Care, Inc was certified by Medicare in 2001 and is operated as a for-profit provider.
7400 Southwest 5oth Terrace Suite 100
Advantis Home Care, Inc
Advantis Home Care, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
2921 Southwest 8 Street
Alegre's Home Health Care, Inc
Alegre's Home Health Care, Inc was certified by Medicare in 2004 and is operated as a for-profit provider.
6187 Northwest 167 Street Suite H34
Aleyda's Home Care, Inc
Aleyda's Home Care, Inc was certified by Medicare in 2004 and is operated as a for-profit provider.
All Around Home Health Agency, Inc
All Around Home Health Agency, Inc was certified by Medicare in 2007 and is operated as a for-profit provider.
275 Fontainebleau Boulevard Suite 120
Alliance Home Health, Inc
Alliance Home Health, Inc was certified by Medicare in 2004 and is operated as a for-profit provider.
7340 Southwest 48th Street Unit 106
All Medical Home Health, Inc
All Medical Home Health, Inc was certified by Medicare in 2007 and is operated as a for-profit provider.
13552 Southwest 128th Street
Alondra Home Help, LLC
Alondra Home Help, LLC was certified by Medicare in 2006 and is operated as a for-profit provider.
13780 Southwest 26th Suite 208
America Home Health, Inc
America Home Health, Inc was certified by Medicare in 2005 and is operated as a for-profit provider.
6595 Northwest 36th Street Suite 222 3
American Care Unit Home Care, Inc
American Care Unit Home Care, Inc was certified by Medicare in 2005 and is operated as a for-profit provider.
3271 North West 7th Street Suite 210
American Home Health Care Corporation
American Home Health Care Corporation was certified by Medicare in 2006 and is operated as a for-profit provider.
11880 Bird Road Suite 402
American Providers, Inc
American Providers, Inc is a 5-star patient rated facility that was certified by Medicare in 1980 and is operated as a for-profit provider.
Rated 5.00 out of 5 from 2 User Reviews
2000 Northwest 89 Place
Amstaff Services, Inc
Amstaff Services, Inc was certified by Medicare in 2005 and is operated as a for-profit provider.
1190 Northeast 163rd Street Suite 310
Angeles Protectores Home Health Care, Inc
Angeles Protectores Home Health Care, Inc was certified by Medicare in 2004 and is operated as a for-profit provider.
16205 Southwest 117 Avenue #26
Angel Home Care Services, Inc
Angel Home Care Services, Inc was certified by Medicare in 2002 and is operated as a for-profit provider.
12955 Southwest 42 Street #104
Antaeus Health Services Corporation
Antaeus Health Services Corporation was certified by Medicare in 2004 and is operated as a for-profit provider.
701 Northwest 57th Avenue Suite 222
Anthony Home Health Care, Corporation
Anthony Home Health Care, Corporation was certified by Medicare in 2004 and is operated as a non-profit provider.
8181 Northwest 36 Street Suite 18
ARC Professional Services
ARC Professional Services was certified by Medicare in 1999 and is operated as a for-profit provider.
1414 Northwest 107th Avenue Suite 102
Ariza Quality Medical Services, Inc
Ariza Quality Medical Services, Inc was certified by Medicare in 2005 and is operated as a for-profit provider.
11401 Southwest 40th Street Suite 211
ASA Home Care Services, Inc
ASA Home Care Services, Inc was certified by Medicare in 2001 and is operated as a for-profit provider.
8700 West Flagler Street Suite 110
Associated Home Health
Associated Home Health was certified by Medicare in 1996 and is operated as a for-profit provider.
10300 Sunset Drive Suite 230
Atlantic Home Care Services, Corporation
Atlantic Home Care Services, Corporation was certified by Medicare in 2003 and is operated as a for-profit provider.
3785 Northwest 82 Avenue Suite 317
Avanti Home Health Services, Inc
Avanti Home Health Services, Inc was certified by Medicare in 2005 and is operated as a for-profit provider.
9730 Northwest 25 Street 2nd Floor
Baptist Health Home Care
Baptist Health Home Care was certified by Medicare in 1992 and is operated as a non-profit provider.
12400 Southwest 127th Avenue
Best Care Agency of Dade County, Inc
Best Care Agency of Dade County, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
666 Northeast 125 Street Suite 231
Best Service Home Health Care, LLC
Best Service Home Health Care, LLC was certified by Medicare in 2004 and is operated as a for-profit provider.
9000 Southwest 87th Court Suite 107B
Bethesta Home Health Care, LLC
Bethesta Home Health Care, LLC was certified by Medicare in 2007 and is operated as a for-profit provider.
B Friends Home Health, Inc
B Friends Home Health, Inc was certified by Medicare in 2007 and is operated as a for-profit provider.
8045 Northwest 36th Street Suite 540
Bluecare Home Health Services, Inc
Bluecare Home Health Services, Inc was certified by Medicare in 2005 and is operated as a for-profit provider.
175 Fontianebleau Boulevard Suite 2M5
Blue Hope Professional Care, Inc
Blue Hope Professional Care, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
2711 Southwest 137 Avenue Suite 79
Calura Home Health Services, Inc
Calura Home Health Services, Inc was certified by Medicare in 2005 and is operated as a for-profit provider.
Care One Home Health, Inc
Care One Home Health, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
5600 Southwest 135th Avenue Suite 211
Care Response Home Health Agency Corporation
Care Response Home Health Agency Corporation is a 5-star patient rated facility that was certified by Medicare in 2004 and is operated as a for-profit provider.
Rated 5.00 out of 5 from 1 User Review
313 Southwest 27th Avenue
Caring Nurse Home Health, Corporation
Caring Nurse Home Health, Corporation was certified by Medicare in 2005 and is operated as a for-profit provider.
6704 Northwest 72 Avenue
Caring Professional Services, Inc
Caring Professional Services, Inc was certified by Medicare in 2005 and is operated as a for-profit provider.
8472 74 Southwest 8th Street
Comfort Care Home Services Corporation
Comfort Care Home Services Corporation was certified by Medicare in 2006 and is operated as a for-profit provider.
12491 Southwest 134 Court Suite 31
D & D & D Home Health Care, Inc
D & D & D Home Health Care, Inc was certified by Medicare in 2007 and is operated as a for-profit provider.
13205 Southwest 137 Avenue Suite 223
DD Health Home Care, Inc
DD Health Home Care, Inc was certified by Medicare in 2001 and is operated by a government entity.
4210 Northwest 4 Street
Demosthenes Home Health Agency, Inc
Demosthenes Home Health Agency, Inc was certified by Medicare in 2005 and is operated as a for-profit provider.
14707 S Dixie Highway Unit 314
D'first Home Care, Inc
D'first Home Care, Inc was certified by Medicare in 2002 and is operated as a for-profit provider.
13062 Southwest 133 Court
Dubet Health Services Corporation
Dubet Health Services Corporation was certified by Medicare in 2004 and is operated as a for-profit provider.
963 Southwest 122nd Avenue
Education Home Health Care Services, Inc
Education Home Health Care Services, Inc was certified by Medicare in 2005 and is operated as a for-profit provider.
400 Southwest 107 Avenue Suite 306A
Emal Professional Services
Emal Professional Services was certified by Medicare in 2002 and is operated as a for-profit provider.
Enery Home Health Care
Enery Home Health Care was certified by Medicare in 2004 and is operated as a for-profit provider.
7570 Northwest 14 Street Suite 113
Exclusive Home Care, Inc
Exclusive Home Care, Inc was certified by Medicare in 2005 and is operated as a for-profit provider.
Exclusive Services, Inc
Exclusive Services, Inc was certified by Medicare in 2003 and is operated as a for-profit provider.
7430 Southwest 41st Street
Faith Health Care, Inc
Faith Health Care, Inc is a 5-star patient rated facility that was certified by Medicare in 2001 and is operated as a for-profit provider.
11401 Southwest 40th Street
Family Home Health Services
Family Home Health Services was certified by Medicare in 2004 and is operated as a for-profit provider.
F & E Home Health Care, Inc
F & E Home Health Care, Inc was certified by Medicare in 2004 and is operated as a for-profit provider.
7175 Southwest 8th Street Suite 213
First Quality Home Care, Inc
First Quality Home Care, Inc was certified by Medicare in 2000 and is operated as a for-profit provider.
First RN, Inc
First RN, Inc was certified by Medicare in 2007 and is operated as a for-profit provider.
15251 Northeast 18th Avenue Suite 12
Five Star Home Health Care, Inc
Five Star Home Health Care, Inc was certified by Medicare in 2006 and is operated as a non-profit provider.
13212 14 Southwest 8th Street
Florida Affordable Home Health Care Corporation
Florida Affordable Home Health Care Corporation was certified by Medicare in 2006 and is operated as a for-profit provider.
Florida Health Care Center, Inc
Florida Health Care Center, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
Florida Home Health Association, Inc
Florida Home Health Association, Inc was certified by Medicare in 2004 and is operated as a non-profit provider.
8180 Doral Boulevard Suite 409
Florida Home Health Care Providers, Inc
Florida Home Health Care Providers, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
4150 Northwest 7th Street Suite 204
GCA Services, Inc
GCA Services, Inc is a 3-star patient rated facility that was certified by Medicare in 2007 and is operated as a for-profit provider.
Gentiva Health Services
Gentiva Health Services was certified by Medicare in 1975 and is operated as a for-profit provider.
7200 Northwest 19th Street Building 4 Suite 114
Gentle Care, Inc
Gentle Care, Inc was certified by Medicare in 2002 and is operated as a for-profit provider.
1790 Southwest 27th Avenue
Gentle Hands Health Care Services
Gentle Hands Health Care Services was certified by Medicare in 2000 and is operated as a for-profit provider.
6840 Southwest 40th Street Suite 212
Global Nursing Home Health, Inc
Global Nursing Home Health, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
Golden Age Home Health, Inc
Golden Age Home Health, Inc was certified by Medicare in 2007 and is operated as a for-profit provider.
10250 Southwest 56 Street Suite A 104
Goldencare Home Health Miami
Goldencare Home Health Miami was certified by Medicare in 2002 and is operated as a for-profit provider.
5757 Blue Lagoon Drive Suite 420
Golden Home Health Care, Inc
Golden Home Health Care, Inc was certified by Medicare in 2007 and is operated as a for-profit provider.
12075 Southwest 131 Avenue
Grand Opportunity Home Health, Inc
Grand Opportunity Home Health, Inc was certified by Medicare in 2007 and is operated as a for-profit provider.
1250 Southwest 27th Avenue Suite 4306
Great Health Care Agency, Inc
Great Health Care Agency, Inc was certified by Medicare in 2004 and is operated as a for-profit provider.
7311 Northwest 12 Street Suite 7
Green Cross Home Care Services, Inc
Green Cross Home Care Services, Inc is a 2-star patient rated facility that was certified by Medicare in 2003 and is operated as a for-profit provider.
15383 Northwest 7th Avenue
Healthcare Unlimited of Florida, Inc
Healthcare Unlimited of Florida, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
7071 Southwest 47th Street
Health Medical Home Care, Inc
Health Medical Home Care, Inc was certified by Medicare in 2001 and is operated as a for-profit provider.
2760 Southwest 97 Avenue Suite 101
Home Advantage of Florida
Home Advantage of Florida is a 4-star patient rated facility that was certified by Medicare in 2004 and is operated as a for-profit provider.
Home Bound Care, Inc
Home Bound Care, Inc was certified by Medicare in 2003 and is operated as a for-profit provider.
300 Northwest 183rd Street
Home Care Services Provider
Home Care Services Provider was certified by Medicare in 2004 and is operated as a for-profit provider.
Home Health Nursing Services
Home Health Nursing Services was certified by Medicare in 2001 and is operated as a for-profit provider.
913 A Southwest 87th Avenue
Hope Home Health Corporation
Hope Home Health Corporation was certified by Medicare in 2006 and is operated as a for-profit provider.
Horizon East Home Care, Inc
Horizon East Home Care, Inc was certified by Medicare in 2005 and is operated as a for-profit provider.
9485 Southwest 72nd Avenue Suite A 245
Humanity Home Health Care, Inc
Humanity Home Health Care, Inc was certified by Medicare in 2007 and is operated as a for-profit provider.
42 Northwest 27th Avenue Suite 315 1
Ideal Home Health, Inc
Ideal Home Health, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
8300 W Flager Street Suite 200
Integrated Health Care Services
Integrated Health Care Services was certified by Medicare in 2006 and is operated as a for-profit provider.
Intercare Home Health Services, Inc
Intercare Home Health Services, Inc was certified by Medicare in 2007 and is operated as a for-profit provider.
10300 Sunset Drive Suite 460 Unit 6
Interim Healthcare
Interim Healthcare was certified by Medicare in 2004 and is operated as a for-profit provider.
1525 Northwest 167 Street Suite 330
International Home Care Service
International Home Care Service was certified by Medicare in 2001 and is operated as a for-profit provider.
10261 Southwest 72nd Street
JDF Home Care, Inc
JDF Home Care, Inc was certified by Medicare in 2004 and is operated as a for-profit provider.
9100 Southwest 24th Street Suite 10
JEM Home Health Care, LLC
JEM Home Health Care, LLC was certified by Medicare in 2004 and is operated as a for-profit provider.
1380 Northeast Miami Gardens Drive Suite 205
Kaerbear's Healthcare, LLC
Kaerbear's Healthcare, LLC was certified by Medicare in 2005 and is operated as a for-profit provider.
1897 Northeast 164 Street
Kassy Home Health Care, Inc
Kassy Home Health Care, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
12855 Southwest 136 Avenue 108
Kendall Comprehensive, Inc
Kendall Comprehensive, Inc was certified by Medicare in 2007 and is operated as a for-profit provider.
11865 Southwest 26th Street Suite I 8
Kidcare Nursing Services
Kidcare Nursing Services was certified by Medicare in 2007 and is operated as a for-profit provider.
99 Northwest 183rd Street Suite 111
LA Caridad Home Health Services Corporation
LA Caridad Home Health Services Corporation was certified by Medicare in 2007 and is operated as a for-profit provider.
8743 Southwest 9th Terrace Suite 4
Larkin Home Health Services, Inc
Larkin Home Health Services, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
Las Mercedes Home Care Corporation
Las Mercedes Home Care Corporation was certified by Medicare in 2001 and is operated as a for-profit provider.
2103 Coral Way Suite 404
Lazaro Home Health Care, Inc
Lazaro Home Health Care, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
Lesly Home Health Care, Inc
Lesly Home Health Care, Inc was certified by Medicare in 2005 and is operated as a for-profit provider.
175 Fontainbleau Boulevard #1r6
Lifeline Home Healthcare Providers, Inc
Lifeline Home Healthcare Providers, Inc was certified by Medicare in 2005 and is operated as a for-profit provider.
8512 Southwest 8th Street Rear
Little Havana Activities & Nutrition Centers
Little Havana Activities & Nutrition Centers was certified by Medicare in 2005 and is operated as a non-profit provider.
Llerena Home Health Care, Inc
Llerena Home Health Care, Inc was certified by Medicare in 2007 and is operated as a for-profit provider.
11890 Southwest 8 Street #201
Longcare Home Health Corporation
Longcare Home Health Corporation was certified by Medicare in 2006 and is operated as a for-profit provider.
10511 Southwest 88 Street Suite C201
Los Jazmines Home Care Corporation
Los Jazmines Home Care Corporation was certified by Medicare in 2005 and is operated as a for-profit provider.
Loving Heart Home Health Care
Loving Heart Home Health Care was certified by Medicare in 2001 and is operated as a for-profit provider.
LRL Home Health Corporation
LRL Home Health Corporation was certified by Medicare in 2005 and is operated as a for-profit provider.
LTC Professional Consultants, Inc
LTC Professional Consultants, Inc was certified by Medicare in 2004 and is operated as a for-profit provider.
7400 Southwest 48th Street Unit 17
Lumar's Health Care Corporation
Lumar's Health Care Corporation was certified by Medicare in 2004 and is operated as a for-profit provider.
7205 Corporate Center Drive #205
MAM Home Health Enterprises, Inc
MAM Home Health Enterprises, Inc was certified by Medicare in 2007 and is operated as a for-profit provider.
199 Southwest 12 Avenue Suite 4
Marcos Home Health Services, Corporation
Marcos Home Health Services, Corporation was certified by Medicare in 2004 and is operated as a for-profit provider.
3905 Southwest 137th Avenue Suite C 2 3
Master Superior Home Care Services, Inc
Master Superior Home Care Services, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
12260 Southwest 8th Street Suite 232
Medex Home Care, Inc
Medex Home Care, Inc was certified by Medicare in 2002 and is operated as a for-profit provider.
8250 Northwest 27th Street
Mediadvantage Home Health Care Services
Mediadvantage Home Health Care Services was certified by Medicare in 2004 and is operated as a for-profit provider.
Mediassist Home Health Care Services Agency Corporation
Mediassist Home Health Care Services Agency Corporation was certified by Medicare in 2004 and is operated as a for-profit provider.
16235 Southwest 117 Avenue #3
Mercy Hospital Home Health Age
Mercy Hospital Home Health Age was certified by Medicare in 1991 and is operated as a non-profit provider.
3663 South Miami Avenue
Merlys Home Health Care Agency, Inc
Merlys Home Health Care Agency, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
7216 Southwest 8th Street Suite 2
MF Home Care Services
MF Home Care Services was certified by Medicare in 2002 and is operated as a for-profit provider.
7035 H Southwest 47th Street
Miami Home Health Agency, Inc
Miami Home Health Agency, Inc was certified by Medicare in 2005 and is operated as a for-profit provider.
13055 Southwest 42 Street Suite 208
MVP Health, Inc
MVP Health, Inc was certified by Medicare in 2007 and is operated as a for-profit provider.
12350 Southwest 132nd Court Suite 212
MYG Home Care Agency
MYG Home Care Agency was certified by Medicare in 2002 and is operated as a for-profit provider.
11398 West Flagler Street Suite 209
Nany Home Health Care
Nany Home Health Care was certified by Medicare in 2002 and is operated as a for-profit provider.
9010 Southwest 137 Avenue 111
Nationwide Healthcare Services, Inc
Nationwide Healthcare Services, Inc was certified by Medicare in 2002 and is operated as a for-profit provider.
18350 Northwest 2nd Avenue Suite 401
New Health Care Corporation
New Health Care Corporation was certified by Medicare in 2004 and is operated as a for-profit provider.
New Life Home Healthcare, Inc
New Life Home Healthcare, Inc was certified by Medicare in 2005 and is operated as a non-profit provider.
Nursemed Home Care Corporation
Nursemed Home Care Corporation was certified by Medicare in 2006 and is operated as a for-profit provider.
2050 Coral Way S 508
Nurse to Go Home Health Care Corporation
Nurse to Go Home Health Care Corporation was certified by Medicare in 2005 and is operated as a for-profit provider.
Nursing Plus, Inc
Nursing Plus, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
Nursing Quality Services, Inc
Nursing Quality Services, Inc was certified by Medicare in 2004 and is operated as a for-profit provider.
8300 Southwest 8 Street Suite 107
Nursing Unlimited 2000, Inc
Nursing Unlimited 2000, Inc was certified by Medicare in 1999 and is operated as a for-profit provider.
4953 Southwest 74th Court
On The Way Home Care, Inc
On The Way Home Care, Inc is a 1.5-star patient rated facility that was certified by Medicare in 2007 and is operated as a for-profit provider.
4005 Northwest 114 Avenue Unit 4
Optima Health Care Services Corporation
Optima Health Care Services Corporation was certified by Medicare in 2006 and is operated as a for-profit provider.
Patient Care, Inc
Patient Care, Inc was certified by Medicare in 2004 and is operated as a for-profit provider.
175 Fountainebleau Boulevard 1 R 2
Patient Resources Company
Patient Resources Company was certified by Medicare in 2005 and is operated as a for-profit provider.
6710 Main Street Suite 234
Patient's Choice Home Health Care, Inc
Patient's Choice Home Health Care, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
PM Home Care, Inc
PM Home Care, Inc was certified by Medicare in 2005 and is operated as a for-profit provider.
1727 Southwest 4th Street
Preferred Care Home Health Services
Preferred Care Home Health Services was certified by Medicare in 2005 and is operated as a for-profit provider.
9065 Southwest 87th Avenue Suite 110
Preferred Home Health Agency, Inc
Preferred Home Health Agency, Inc is a 5-star patient rated facility that was certified by Medicare in 2006 and is operated as a for-profit provider.
Preferred Home Health Care, Inc
Preferred Home Health Care, Inc was certified by Medicare in 2004 and is operated as a for-profit provider.
4929 Southwest 74 Court
Premier Plus Home Health
Premier Plus Home Health was certified by Medicare in 2003 and is operated as a for-profit provider.
3100 Northwest 72nd Avenue Unit 125
Premium Health Services Corporation
Premium Health Services Corporation is a 5-star patient rated facility that was certified by Medicare in 2006 and is operated as a for-profit provider.
12002 Southwest 128 Court Suite 102
Premium Home Health Care, Inc
Premium Home Health Care, Inc was certified by Medicare in 2004 and is operated as a for-profit provider.
Prestige Home Health Services Corporation
Prestige Home Health Services Corporation was certified by Medicare in 2006 and is operated as a for-profit provider.
7220 Northwest 36th Street Suite 307 A
Prime Care Health Agency, Inc
Prime Care Health Agency, Inc was certified by Medicare in 2002 and is operated as a for-profit provider.
8405 Northwest 53rd Avenue Suite B 106
Priority Home Health, Inc
Priority Home Health, Inc was certified by Medicare in 2003 and is operated as a for-profit provider.
175 Fontainebleau Boulevard Suite 2 J 3
QA Nursing Services Corporation
QA Nursing Services Corporation was certified by Medicare in 2005 and is operated as a for-profit provider.
Quali Care Home Health Agency
Quali Care Home Health Agency was certified by Medicare in 2002 and is operated as a for-profit provider.
18001 Old Cutter Road Suite 421
Quality Professional Health Care, Inc
Quality Professional Health Care, Inc was certified by Medicare in 2007 and is operated as a for-profit provider.
RB Home Health Services, Inc
RB Home Health Services, Inc is a 5-star patient rated facility that was certified by Medicare in 2003 and is operated as a for-profit provider.
2711 Southwest 137th Avenue #90
Reality Care Home Health Services, Inc
Reality Care Home Health Services, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
Renaissance Home Health Care, Inc
Renaissance Home Health Care, Inc was certified by Medicare in 2005 and is operated as a non-profit provider.
12233 Southwest 132nd Court
Renovation Home Health Care, Inc
Renovation Home Health Care, Inc is a 5-star patient rated facility that was certified by Medicare in 2007 and is operated as a for-profit provider.
R & N Professional Services Corporation
R & N Professional Services Corporation was certified by Medicare in 2006 and is operated as a for-profit provider.
6555 Northwest 36th Street Suite 201F
Santa Fe Home Health Care, Inc
Santa Fe Home Health Care, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
8181 Northwest 36th Street Suite 7
Santa Teresita Home Care Corporation
Santa Teresita Home Care Corporation was certified by Medicare in 2005 and is operated as a for-profit provider.
Serendipity Home Health, Inc
Serendipity Home Health, Inc was certified by Medicare in 2007 and is operated by a government entity.
2141 Southwest 1st Street Suite 104
Serenity Home Health Care, Inc
Serenity Home Health Care, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
Services & Care at Home
Services & Care at Home was certified by Medicare in 2002 and is operated as a for-profit provider.
10250 Southwest 56 Street D103
Skill Home Health Care Corporation
Skill Home Health Care Corporation was certified by Medicare in 2005 and is operated as a for-profit provider.
Southeast Homecare Corporation
Southeast Homecare Corporation was certified by Medicare in 2003 and is operated as a for-profit provider.
South Florida Home Health Care, Inc
South Florida Home Health Care, Inc was certified by Medicare in 2004 and is operated as a for-profit provider.
St. Jude Health Care, Inc
St. Jude Health Care, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
6356 Manor Lane Suite 101
Sunlight Home Care, Inc
Sunlight Home Care, Inc was certified by Medicare in 2005 and is operated as a for-profit provider.
400 Southwest 107 Avenue Suite 404
Sunrise Home Health Care, Inc
Sunrise Home Health Care, Inc was certified by Medicare in 2001 and is operated as a for-profit provider.
2331 Southwest 82 Place
Sunset Home Healthcare, Inc
Sunset Home Healthcare, Inc was certified by Medicare in 2007 and is operated as a for-profit provider.
275 Fontainebleu Boulevard Suite 215
Sunshine Home Care Agency, Inc
Sunshine Home Care Agency, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
Sweet Angels Health Services, Inc
Sweet Angels Health Services, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
Sweet Care Home Health Agency, Inc
Sweet Care Home Health Agency, Inc was certified by Medicare in 2004 and is operated as a for-profit provider.
Sweet Home Services, Inc
Sweet Home Services, Inc was certified by Medicare in 2007 and is operated as a for-profit provider.
1865 Brickell Avenue A 209
Tehc, LLC
Tehc, LLC was certified by Medicare in 2003 and is operated as a for-profit provider.
Tender Care Home Health Services
Tender Care Home Health Services was certified by Medicare in 2001 and is operated as a for-profit provider.
8875 Northwest 23 Street Unit A
Tender Touch Home Health, LLC
Tender Touch Home Health, LLC is a 1-star patient rated facility that was certified by Medicare in 2004 and is operated as a for-profit provider.
The Healing Care, Inc
The Healing Care, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
12956 Southwest 133rd Court Suite B
Total Care Home Services, Inc
Total Care Home Services, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
Total Home Health Care, Inc
Total Home Health Care, Inc is a 4-star patient rated facility that was certified by Medicare in 2003 and is operated as a for-profit provider.
Total Nursing Services, Inc
Total Nursing Services, Inc was certified by Medicare in 2003 and is operated as a for-profit provider.
5951 Northwest 173rd Drive Suite 11
Tropical Health & Homecare Services, Inc
Tropical Health & Homecare Services, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
160 Northwest 176th Street Suite 309
Trust Care Home Health Services, Inc
Trust Care Home Health Services, Inc was certified by Medicare in 2006 and is operated as a for-profit provider.
2885 Southwest 3 Avenue Suite 100
Unisource Home Health Services
Unisource Home Health Services was certified by Medicare in 2002 and is operated as a for-profit provider.
7440 Southwest 50 Terrace Suite 104
United Home Care Services, Inc
United Home Care Services, Inc was certified by Medicare in 1999 and is operated as a non-profit provider.
5255 Northwest 87th Avenue Suite 301
Universal Home Healthcare, Inc
Universal Home Healthcare, Inc is a 5-star patient rated facility that was certified by Medicare in 2006 and is operated as a for-profit provider.
8603 South Dixie Highway Suite 310
Unlimited Care of Florida, Inc
Unlimited Care of Florida, Inc was certified by Medicare in 2004 and is operated as a for-profit provider.
11890 Southwest 8 Street Suite 401
Unlimited Home Care, Inc
Unlimited Home Care, Inc was certified by Medicare in 2005 and is operated as a for-profit provider.
454 Northwest 22 Avenue Suite 201
Virgin Health Corporation, Inc
Virgin Health Corporation, Inc is a 5-star patient rated facility that was certified by Medicare in 2006 and is operated as a for-profit provider.
7300 Corporate Center Drive Suite 702
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Miami at a Glance
Miami has a total population of 362,470, of which 78,797 are children under the age of 18 and 61,768 are seniors 65 and older. The median age is 37.7.
Total Population:
Median Age:
180,194 (49.7%)
Children (0-17):
78,797 (21.7%)
Adults (18-64):
Seniors (65+):
Age Breakdown:
Divorced:
Marriage Breakdown:
Hispanic Ethnicity:
238,351 (65.76%)
80,858 (22.31%)
Asian:
2,376 (0.66%)
Pacific Islander:
130 (0.04%)
Indian:
19,644 (5.42%)
Two or More:
The average number of disabilities per resident is 0.50, which does not include institutionalized individuals.
Disabilities:
0.50 (Per Capita)
Dialysis Centers:
Home Agencies:
Nursing Homes:
Medical Suppliers:
Rehab Centers:
The median family income is $27,225 while the median household income is $23,483. Roughly 27.70% of the population live in poverty.
Family Income:
Household Income:
In Poverty:


Those of us who followed the Swans in the 1960s and early 1970s will have been saddened by the news of the death of Brian Evans. Rather like the death of a relative or friend, Brian's passing signals just another little piece of the past disappearing for many of us.
I was first taken to the Vetch in April 1968 and would have seen him play that evening. In truth, my eyes were probably more directed toward Ivor Allchurch in that particular game, but over the coming seasons the little curly haired winger was to become crucial to my enjoyment of the team and the football they played.
I was aware that Brian had played for the Swans in the old second division, and was a member of the legendary 1964 FA Cup Semi-Final squad. Later searches of the record books showed that he was one of the heroes of Anfield in that epic run, and had also played before the record Vetch Field crowd against Arsenal in 1968. However, personally, Brian will always be identified as a vital component of Roy Bentley's team that first really got me hooked as a life-long Swans fan.
In truth, many of my first few visits to the Vetch had left me underwhelmed, but from early on I appreciated the attacking skills and ball control of the man from Abergavenny. You always knew that if Brian got the ball something could happen. Without need to recourse to record books, I can still mentally picture a solo effort he scored against Lincoln in a 5-0 romp in 1968-9, as he bamboozled a couple of defenders in front of the North Bank before shooting into the double-decker end goal.
When Roy Bentley became manager in the summer 1969, Brian was to fit glove-like into his philosophy of attacking football featuring two out and out wingers. Along with Lenny Allchurch, Brian provided a stream of inviting crosses for the likes of Dai Gwyther and Herbie Williams to feast on. The club won promotion in 1970 and consolidated the following year.
Brian was indispensable to that side and if for any reason he was unable to play, the Swans seemed less of a force without him. One memorable sequence of successive home wins over Exeter (4-1), Rochdale (4-2), Telford (6-2), Fulham (4-1) and Rhyl (6-1) speaks more eloquently about the style of play of that team than a thousand words. We almost took it for granted that at some stage Brian would have the crowd roaring with excitement as he beat his man with some piece of close control before firing in a cross or shot.
With the retirement of Lenny Allchurch, Brian became more crucial than ever to the team's creativity. He continued to torment defenders in season 1971-72, and showed his versatility by switching wings to accommodate Ronnie Rees who arrived later that season. Sadly, the team were in decline by that stage, and Brian's final season at the club ended with relegation.
By then a full international, Brian was sold to a then ascendant Hereford United in Harry Gregg's rebuilding over the summer of 1973. He spent his final professional seasons with the border club before returning to West Wales to earn a Welsh League Championship with Llanelli.
Brian also deservedly appeared for Wales, earning his first cap in a 3-0 win over Finland at his home ground. My personal abiding memory of Brian in a Welsh shirt was his part in the goal scored by John Toshack in a 1-1 draw with England in a World Cup Qualifier at Wembley. He also played a major role in the 2-0 win over Poland at Cardiff a few months later, an outstanding result against the side that were to finish third in the 1974 World Cup.
Probably the best eulogy I can give Brian is that he was part and parcel of the first Swans side that I genuinely looked forward to seeing play. With him dies another little piece of growing up.
Thankfully, the memories will live on in the minds of those of us who saw him play. The entertaining attacking play of the early Bentley area turned me into a Swans fan. Brian Evans was indispensable to that side and helped keep me coming back to the Vetch. I don't think you could say much more about a player.


Waste water treatment at 28 of Ireland's 179 large towns and cities has failed to meet standards set to prevent pollution and protect public health.
Waste water from 57 areas caused significant impacts on our rivers, lakes and coastal waters. Discharges of raw sewage from six urban areas have ceased. However, raw sewage from the equivalent of 88,000 people in 38 towns and villages is still flowing into the environment today.
Though we have seen some improvements, Ireland is not investing quickly enough to provide the infrastructure needed to treat our waste water, highlights the EPA report on Urban Waste Water Treatment in 2017; released today. Deficiencies exist in many treatment plants and public sewers, due to a legacy of underinvestment, and waste water is still entering the environment without receiving sufficient treatment.
It is not possible to fix all the issues with Ireland's waste water treatment systems in the short term and a long-term strategy is now required to address shortcomings. It is therefore essential that the resources that are available are targeted efficiently in the right areas, to deliver improvements where they are most needed. The EPA identifies the following as the priority areas for improvements.
28 large towns and cities where waste water treatment failed to meet mandatory standards. These account for over half of the sewage collected in our public sewers. The final deadline to comply with the standards was 2005 and Ireland is before the EU Court of Justice for breaching these requirements.
38 towns and villages discharging raw sewage. The EPA has prosecuted Irish Water for delays in providing treatment plants at six of these areas.
57 areas where waste water discharges are the sole environmental threat to rivers, lakes and coastal waters at risk of pollution.
Areas where upgrade works are needed to protect 4 beaches with poor quality bathing water. These affected beaches are Merrion Strand, Clifden, Loughshinny and Sandymount Strand.
15 areas where improvements are needed to protect critically endangered freshwater pearl mussels or to safeguard shellfish habitats.
13 priority waste water collection networks (sewers) that need to be upgraded.


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'Obstruction' on railway line between Haywards Heath and Lewes causes delays
An 'obstruction' on the railway line between Haywards Heath and Lewes is causing delays.
By Jennifer Logan
Thursday, 20th February 2020, 4:05 pm
Southern rail said the line towards Lewes is currently blocked and as a result, services from Haywards Heath to Eastbourne/Ore via Lewes are being diverted via Brighton.
It confirmed services from Ore/Eastbourne via Lewes to Haywards Heath are running as scheduled.
A spokesman said on Twitter: "If you are travelling to Cooksbridge or Plumpton from Haywards Heath, please travel down to Lewes on the services being diverted to Brighton and change at Lewes for a train services back up to these stations.
There is disruption on the railway line between Haywards Heath and Lewes
"If you are travelling on the services that are being diverted via Brighton to Lewes stations on to Eastbourne and Ore, please allow for extra time to complete your journey."
Engineers are said to be en route to remove the obstruction on the line.

redpajama_set_name: RedPajamaCommonCrawl


Home / Articles / Yemen ceasefire: What Chance for Peace?
Yemen ceasefire: What Chance for Peace?
One of the main impediments in the way of peace in Yemen since the beginning of the Saudi-led invasion in March 2015 has been the difficulty of arranging diplomatic negotiations between the two sides.
Not because Ansarullah, or the National Salvation Government in Sana'a was averse to the idea of speaking to the rulers of Saudi Arabia or the United Arab Emirates (UAE), despite the two countries being responsible for causing the biggest humanitarian catastrophe in living memory. The issue was quite simply that Yemeni negotiators, at least those not on the Saudi payroll, were often completely unable to leave the country in order to attend any diplomatic summit in the first place.
From detaining Yemeni diplomats for months on end in the East African country of Djibouti, to deliberately refusing to grant safe passage guarantees to a chartered Omani plane carrying negotiators from Sana'a who were trying to get to the Geneva talks in September 2018, the Saudi-led invaders have tried everything they could to make negotiations impossible.
It is only thanks to the endless patience and tenacity of the Yemeni people, the dedication to peace voiced over and over again by leaders such as Sayyid 'Abd al-Malik al-Huthi and President Mahdi al-Mashat, and the admittedly praiseworthy work of UN envoy to Yemen Martin Griffiths, that finally real peace negotiations were able to take place in Sweden, in December of 2018.
These negotiations eventually bore fruit: an agreement was signed the same month for a full ceasefire in Hodaydah, the establishment of humanitarian corridors to the suffering people of Yemen, and the deployment of UN observers to safeguard the region.
Furthermore, a "political framework" was set up that was to be discussed in a new round of negotiations in January 2019 (this new round had not yet started at the time of writing, although Jordan has expressed interest in hosting the summit).
However, the question that must be asked, and particularly in the case of Saudi Arabia: is the agreement being respected?
On December 18, Brigadier General Yahya Sari', official spokesperson of the Yemeni Armed Forces, announced that the troops would stand down and respect a total ceasefire in and around Hodaydah. This was followed in early January by a proposal by Muhammad 'Alial-Huthi for the withdrawal and redeployment of all armed forces. By December 31, Yemeni forces had withdrawn in accordance with the ceasefire deal, and even handed over control of the port of Hodaydah to the UN-appointed Head of Monitoring Mission, a retired Dutch general, Patrick Cammaert.
None of this has apparently stopped the bloodshed. The Saudis have reportedly ignored al-Huthi's proposal for withdrawal and violence has continued in Hodaydah.
On December 30, it was reported that Saudi-backed forces carried out no fewer than 36 raids. Further, 28 artillery shells were fired at Hodaydah in a matter of a single day. From January 9–13, the number of shells and missiles launched reached 405; and on January 17, General Sari' reported that Saudi forces had fired 329 explosives during the previous three days.
At the same time, invading forces from the UAE started building fortifications and ramparts, indicating that they are preparing for new battles in the future. Not only is this a violation of the spirit of the ceasefire, it also clearly proves that the Emiratis are not planning to withdraw or redeploy their forces as they agreed to in Sweden.
Saudi/American proxy, Yemeni Foreign Minister Khalid al-Yamani, (left) and head negotiator for the legitimate interim government of Yemen, Muhammad 'Abd al-Salam (right) shake hands under the eyes of UN Secretary-General António Guterres, during peace talks at Johannesberg Castle in Rimbo, Sweden. The ceasefire agreement, however, only applies to the port of Hodaydah, which all subsequent indications suggest is not being honored by the aggressors (UAE, Saudi Arabia, and by extension the US), who continue to shell not only Hodaydah, in open violation of the ceasefire, but the rest of the country. The collapsed economy and the extended disruption to food and fuel supplies coming through the main port at Hodaydah could have had devastating consequences for the most vulnerable. An extra one million children now risk falling into famine, bringing the total to 5.2 million.
The invaders have also leveled unfounded allegations against Ansarullah and the National Salvation Government, even going as far as to accuse them of blocking humanitarian aid from entering the Hodaydah port. This accusation is made despite the fact that it was the government in Sana'a that for years has pleaded to have the Hodaydah port accessible to much-needed aid.
Meanwhile, the UN-appointed retired General Cammaert, who was supposed to ensure that the agreement signed in Sweden is adhered to fully, has lost the trust of the Yemeni people. On January 13, Yemen's chief negotiator Muhammad 'Abd al-Salam accused the UN officer of "deviating from the Agreement" in response to the general's inability to keep the aggression forces in check and prevent further bloodshed in and around Hodaydah.
Even the humanitarian corridor system has been barely effective. While some increase in flow of goods to the Hodaydah port and from there to the hinterland of Yemen has occurred, there is still too little improvement for the starving and suffering inhabitants, particularly those of northern Yemen. The UN Monitoring Mission has been unable to prevent attacks taking place in territories that nominally fall under the humanitarian corridor, making the delivery of goods that arrive in Hodaydah to other parts of the country very difficult.
When the agreements were signed, the National Salvation Government proposed opening a safe road from the Red Sea wheat mills in Hodaydah to Sana'a, in order to alleviate the suffering of the people there. In a shock decision on January 3, Saudi representatives rejected the proposal and refused to guarantee safe passage to the wheat delivery transports. And on January 11, UN Humanitarian Coordinator for Yemen, Lise Grande, visited Hodaydah and called for urgent measures to ensure safe transportation of aid, showcasing that even weeks after the agreement was signed in Sweden, the corridors remained largely ineffective.
Last but not least, the UAE and Saudi regimes have refused the exchange of prisoners as agreed to earlier. While Riyadh released a list of prisoners they are willing to release, hundreds of names of Yemeni troops and civilians who were reportedly taken prisoner were not on the list. The Saudi regime refused to even acknowledge that they hold them prisoner.
The ceasefire that was signed amid high hopes and expectations in Sweden has so far failed to deliver most of its promises. The fault lies entirely with the invading coalition.
It is important to remember that the ceasefire, even with all the violations by the Saudi-led invaders, only applies to Hodaydah and its surroundings. The rest of Yemen is still subject to the most horrific crimes perpetrated by the aggressors. From the use of illegal chemical weapons in Sa'ada leading to fetal deaths and horrible congenital deformity to the expulsion of the tribes of Mahrah in order to make room for a planned Saudi oil pipeline to the coastline, all of Yemen is feeling the jackboot of imperialist aggression just as harshly as ever.
Until the international community gets serious about ensuring the Saudis abide by humanitarian law, the UN mission in Yemen strictly enforces the agreement on the Saudis and Emiratis, Western powers finally cut weapons exports and their continued support to both the Saudis and the Emiratis, the chances for a negotiated peace in Yemen remain extremely slim.
Brecht Jonkers specialises in the history of the Muslim East.


The endocannabinoid system has been implicated in several neurobiological processes, including neurodegeneration, neuroprotection and neuronal plasticity. The CB1 cannabinoid receptors are abundantly expressed in the basal ganglia, the circuitry that is mostly affected in Parkinson's Disease (PD). Some studies show variation of CB1 expression in basal ganglia in different animal models of PD, however the results are quite controversial, due to the differences in the procedures employed to induce the parkinsonism and the periods analyzed after the lesion. The present study evaluated the CB1 expression in four basal ganglia structures, namely striatum, external globus pallidus (EGP), internal globus pallidus (IGP) and substantia nigra pars reticulata (SNpr) of rats 1, 5, 10, 20, and 60 days after unilateral intrastriatal 6-hydroxydopamine injections, that causes retrograde dopaminergic degeneration. We also investigated tyrosine hydroxylase (TH), parvalbumin, calbindin and glutamic acid decarboxylase (GAD) expression to verify the status of dopaminergic and GABAergic systems. We observed a structure-specific modulation of CB1 expression at different periods after lesions. In general, there were no changes in the striatum, decreased CB1 in IGP and SNpr and increased CB1 in EGP, but this increase was not sustained over time. No changes in GAD and parvalbumin expression were observed in basal ganglia, whereas TH levels were decreased and the calbindin increased in striatum in short periods after lesion. We believe that the structure-specific variation of CB1 in basal ganglia in the 6-hydroxydopamine PD model could be related to a compensatory process involving the GABAergic transmission, which is impaired due to the lack of dopamine. Our data, therefore, suggest that the changes of CB1 and calbindin expression may represent a plasticity process in this PD model.
Copyright: © 2013 Chaves-Kirsten et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: FAPESP CNPq University of São Paulo - NAPNA . The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
The cannabinoid compounds are lipophilic molecules which exert their effects by binding to specific membrane receptors . Two types of cannabinoid receptors, both coupled to G proteins, have been identified (CB1 and CB2). These two receptors control peripheral and central functions [2,3]. In addition, more recently it has been shown that cannabinoids can also bind to other types of receptors, such as the transient receptor potential vanilloid-1 (TRPV1)  and peroxisome proliferator-activated receptor (PPAR) family of nuclear receptors . Endocannabinoids are usually released from target neurons and act as retrograde messengers that regulate synaptic transmission. The activation of presynaptic CB1 results in inhibition of the release of some neurotransmitters, such as glutamate and γ-aminobutyric acid (GABA) [6,7].
High amounts of CB1 are found in the basal ganglia [substantia nigra (SN), globus pallidus (GP), entopeduncular nucleus and lateral striatum], cerebellum, and hippocampus [1,3,8]. In the striatum, the highest expression of CB1 occurs in its dorsolateral portion  mainly in the terminals of cortical projection neurons and in GABAergic interneurons. In SN, CB1 receptors are located in the terminals of spiny striatal neurons in the pars reticulata (SNpr). Dopaminergic projections from SN innervate the striatal neurons that express CB1 and the dopamine receptors D1 and D2. The D2 and CB1 receptors share a group of G proteins, indicating a convergence of their transduction mechanisms. On the other hand, the activation of D1 receptors, mediated by adenylyl cyclase, can be completely blocked by CB1 stimulation. In the medial portion of globus pallidus (also known as internal globus pallidus – IGP) and in the SNpr it is well established that the activation of CB1 reduces the release of both GABA and glutamate from terminals originating in the striatum and subthalamic nucleus, respectively [10–14]. In addition to the high expression of CB1 in the basal ganglia, endocannabinoid ligands and their synthesizing and degrading enzymes are also particularly abundant in those structures .
Parkinson's disease (PD) is a neurodegenerative disorder associated with loss of 50 to 70% of dopaminergic neurons in the SN pars compacta (SNpc), which has been extensively investigated in regard to its behavioral and molecular aspects, both in animal models and humans [16,17]. The loss of dopamine in the projection area of the SNpc neurons leads to a functional change in the complex circuitry of the basal ganglia , which results in an excessive inhibition of motor systems . The high density of CB1 receptors and endocannabinoids found in the basal ganglia has been a much explored research field that seeks to understand the relation between PD and the cannabinoid system, which has led to prospects for cannabinoid therapies. Indeed, several studies have shown the participation of cannabinoid system in different kinds of neurodegenerative diseases and suggested its neuroprotective properties [20–23]. A recent study with humans, for instance, showed a marked decrease of CB1 in the SN of PD patients, concomitant with a slight increase in dopaminergic projection areas . Delta9-tetrahydrocannabinol (delta9-THC) is able to reverse the decreased dopaminergic transmission in the basal ganglia of a mice model of PD .
Studies employing different animal models of PD, such as 6-hydroxydopamine (6-OHDA) injections in basal ganglia or intracerebroventricular in rats [26–29], intraperitoneal injections of heroin contaminant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in marmosets and mice , and specific park genes deleted- mice , for example, have also reported changes of CB1 expression in the basal ganglia. However, the data are heterogeneous and often conflicting. Those heterogeneous results seem to depend on the procedures employed to induce parkinsonism and the periods analyzed after the lesion .
Temporal variation of CB1 expression during PD progression is poorly understood. Furthermore, most studies are devoted to evaluate CB1 variation focusing on the striatum and SN, and giving minor attention to the other basal ganglia structures, such as external and internal globus pallidus (EGP and IGP, respectively – ). Therefore, the aim of this study was to analyze the time course of CB1 receptor expression by immunoshistochemistry in four structures of basal ganglia, namely striatum, EGP, IGP, and SN, in the PD model of unilateral intraestriatal injections of 6-OHDA in rats. The 6-OHDA injection directly into the striatum causes retrograde dopaminergic degeneration . We also evaluated the expression of tyrosine hydroxylase (TH), glutamic acid decarboxylase (GAD), parvalbumin, and calbindin, by immunoshistochemistry and/or immunoblotting, in an attempt to establish relationships between the cannabinoid system and the dopaminergic and GABAergic systems.
Seventy-days-old male Wistar rats weighting 230-280g at the beginning of the experiments, provided by the central animal house of the Institute of Biomedical Sciences, University of São Paulo, were used in this study. The animals were housed in groups of 3–4 animals per cage, maintained at 23 °C ± 2, in a 12 h light/12 h dark cycle (lights on at 06:00 h), with free access to food and water. The experiments were carried out in accordance with the guidelines of the Brazilian College for Animal Experimentation (COBEA) and were approved by The Ethics Committee for Animal Research of the Institute of Biomedical Sciences, University of São Paulo (Protocol n° 27/68/2), which are in accordance with the procedures of national and international care of animals used in scientific research.
Independent groups of rats were used to investigate the time course effects of 6-OHDA striatal injection on protein levels by immunohistochemical and immunoblotting analysis.
Rats were anesthetized with 2,2,2-tribromoethanol (1 mL/100 g -250 mg/kg i.p. - Sigma®) and placed in a stereotaxic frame (David Kopf Instruments). After craniotomy, two 0.5 µl injections containing 6 µg of 6-OHDA in saline and 0.3% ascorbic acid (totalizing a final dose of 12 µg) were made in the right striatum by way of glass micropipettes coupled to a pressure system, in the following coordinates: (1) AP: bregma, ML: -2.7, and DV: -4.5mm, (2) AP: -0.5, ML: -3.4, and DV: 4 mm . Once the infusion was finished, the micropipette was maintained still in the infused region for approximately one minute to avoid solution reflux, and then it was slowly removed from the brain. The incision was then sutured and treated with Fibrase® (Pfizer) in order to improve healing. The brains of PD-induced rats were then analyzed after 1, 5, 10, 20, and 60 days of the 6-OHDA injections (days post-lesion, DPL). The basal ganglia structures of the lesioned side (right) were always compared to their corresponding in the intact side (left).
PD-induced rats were deeply anesthetized with ketamine (5 mg/100 g of body weight, im) and xylazine (1 mg/100 g of body weight, im), and perfused through the left ventricle with phosphate-buffered saline and 4% paraformaldehyde in 0.1 M phosphate buffer (PB, pH 7.4). The brains were dissected out and after 4-6 hours post-fixation in paraformaldehyde solution they were transferred to a 30% sucrose PB solution to ensure cryoprotection. Coronal sections (30 µm) were then obtained on a sliding microtome and collected in PB.
Sections containing substantia nigra (SN), striatum and globus pallidus (GP) regions were incubated with rabbit polyclonal antiserum anti-CB1 (Cayman, Ann Arbor, MI, USA, 1:1,000), a mouse monoclonal anti-tyrosine hydroxylase antibody (TH; Chemicon, Temecula, CA, USA, 1:1,000) as an indicator of dopaminergic neurons in basal ganglia; a mouse monoclonal anti-parvalbumin antibody (Sigma®; 1: 1,000), and a mouse monoclonal anti-calbindin antibody (Sigma®; 1: 1,000), as indicators of GABAergic neurons in striatum, in PB containing 0.3% Triton X-100 plus 5% of normal goat or donkey sera. Parvalbumin is known to be present in GABAergic neurons in the basal ganglia [34,35]. Immunolabeling with peroxidase methods was conducted as previously described . Controls for CB1 staining included: (1) omission of the primary antibody and (2) preadsorption of the primary antibody overnight with a 10-fold excess of the corresponding control peptide for CB1 (Cayman).
Digital images were acquired using a Nikon E1000 microscope (Melville, NY, USA) and Nikon DMX1200 digital camera (Nikon Imaging Software ACT-U). Images from striatum were captured between bregmas 1.80 and -0.36; from EGP between bregmas -0.24 and -3.12; from IGP between bregmas -1.92 and -2.76; and from SNpc and SNpr between bregmas -4.56 to -6.60 (4-8 sections/brain/structure; n= 4-5 per DPL) . All structures were analyzed by obtaining images at certain intervals between each other in order to represent its entire length, thus ensuring an overview of each structure. Representative images were mounted with Adobe Photoshop (Adobe Systems Inc., Mountain View, CA, USA).
The TH expression was quantified in the striatum (6 sections) and SNpc (6-8 sections) as an indicator of the lesion extension. Parvalbumin and calbindin were quantified in the striatum (6 sections), parvalbumin in dorsolateral striatum and calbindin in ventromedial striatum. CB1 receptor expression was quantified in the striatum (6 sections), EGP (4 sections), IGP (4 sections), and SNpr (6 sections), all carried out with ImageJ (NIH/USA). For TH in SNpc, CB1 in EGP, IGP and SNpr, we measured the integrated density of immunolabeling and of the background (nonlabeled areas) from each slice. The background integrated density was deduced from the integrated density quantification of the labeled areas, to obtain a labeling index reflecting the signal-to-noise ratio. For CB1 immunostaining in the striatum the average of the integrated density of three areas of 2500 µm2 was conducted. For parvalbumin and calbindin in the striatum, positive cells were directly counted. After the quantification blind researchers to the experimental conditions (side and days after lesion) reviewed the data. The resulting indexes were always normalized to the controls.
At the same time points described above, the rats (n=6-8 per group) were sacrificed by cervical dislocation, and the SN (bregma -4.56 to -6.60 below colliculus approximately), and striatum (bregma +2.28 to -1.32, approximately)  were rapidly collected. The immunoblotting assay was conducted as previously described . In short, samples containing 30–40 µg protein were subjected to a 10% acrylamide gel containing sodium dodecyl sulfate and electrotransferred to nitrocellulose membranes using a Trans-Blot cell system (Bio-Rad). The membranes were then blocked for at least 2 hr and incubated overnight with the antibodies against TH or a rabbit policlonal antibody anti-GAD (Millipore, Temecula, CA, USA). Loading control with β-actin was conducted in all experiments by using a mouse monoclonal antibody against β-actin (Sigma, St. Louis, MO). Optical density obtained from TH and GAD was first normalized in relation to the corresponding β-actin bands in each experiment. Subsequently, the normalized data were treated to evaluate protein levels changes in the experimental side in relation to their controls for each time point.
As described for immunohistochemistry, the TH protein levels were quantified by the immunoblotting method as an indication of the lesion extension. GAD levels were investigated in the striatum and SN to obtain indirect data on GABAergic neurons. After the quantification blind researchers to the experimental conditions (side and days after lesion) reviewed the data.
Quantitative data were submitted to statistical analysis using GraphPad Prism 5 (San Diego, CA). The comparisons between control and experimental sides from each group were made using the Paired Student's t-test. The comparisons between all groups were made using the One-Way ANOVA test, followed by Tukey's post-test when appropriate. For all tests described, the significance value adopted was p≤0.05. All data were normalized to the controls and are expressed as means ± SEM.
The analysis of TH, GAD, parvalbumin, calbindin and CB1 protein expression is summarized in Table 1 (immunoblotting) and in Table 2 (immunohistochemistry), and described in detail below. Representative digital images are shown in Figures 1-5.
Table 1. Immunoblotting analysis of TH and GAD expression in the basal ganglia of rats after 1, 5, 10, 20, and 60 days of the 6-OHDA injections (days post-lesion, DPL).
Table 2. Immunohistochemistry analysis of TH, CB1, parvalbumin and calbindin expression in the basal ganglia of rats after 1, 5, 10, 20, and 60 days of the 6-OHDA injections (days post-lesion, DPL).
Figure 1. Temporal changes of TH levels in the striatum of PD-induced rats.
TH levels in striatum of rats submitted to unilateral intrastriatal injections of 6-OHDA after 1, 5, 10, 20, and 60 days post-lesion (DPL). (A) Digital images of coronal sections of the dorsolateral striatum shows a decrease in the expression of TH on the 6-OHDA side, with a peak in 10 DPL (B) Digital images of coronal sections of the dorsolateral striatum at 60 DPL; the arrow indicates the site of infusion. Note the emergence of TH+ cells in the experimental side. (C) Semi-quantitative analysis of TH staining represented as percentage. Control side (dashed line). Statistical analysis by ANOVA (one way) with Tukey post-test. * p <0.05, ** p <0.01 and *** p <0.001.
Figure 2. Temporal changes of TH expression in the SNPc of PD-induced rats.
TH expression in SNpc of rats submitted to unilateral intrastriatal injections of 6-OHDA after 1, 5, 10, 20 and 60 days post-lesion (DPL). (A) Digital images of coronal sections of the SNpc show a progressive decreased TH expression in 6-OHDA side. (B) Semi-quantitative analysis of TH staining represented as percentage. Control group (dashed line). Statistical analysis by ANOVA (one way) with Tukey post-test. * p <0.05, ** p <0.01 and *** p <0.001.
Figure 3. Temporal changes of CB1 expression in the EGP of PD-induced rats.
CB1 expression in external globus pallidus (EGP) of rats submitted to unilateral intrastriatal injections of 6-OHDA after 1, 5, 10, 20, and 60 days post-lesion (DPL). Digital images of coronal sections of the EGP show an increase of CB1 expression in the experimental side at earlier time points.
Figure 4. Temporal changes of CB1 expression in the IGP of PD-induced rats.
CB1 expression in internal globus pallidus (IGP) of rats submitted to unilateral intrastriatal injections of 6-OHDA after 1, 5, 10, 20 and 60 days post-lesion (DPL). Digital images of coronal sections of the IGP show an increase in the CB1 expression in the experimental side at 1 DPL. From 5 to 60 DPL, there was a gradual decrease in the CB1 expression.
Figure 5. Temporal changes of CB1 expression in the SNpr of PD-induced rats.
CB1 expression in the substantia nigra pars reticulata (SNpr) of rats submitted to unilateral intrastriatal injections of 6-OHDA after 1, 5, 10, 20 and 60 days post-lesion (DPL). Digital images of coronal sections of the SNpr show a decrease in the CB1 expression in the experimental side from 5 DPL to 60 DPL.
In general, 6-OHDA produced a decreased TH immunoreactivity in the injured striatum and SNpc compared to control side. In the striatum, the 6-OHDA produced a gradual decrease in the TH immunoreactivity, which was more pronounced at 10 DPL, followed by a slight increase at 20 and 60 DPL (Table 2, Figure 1A). The mean percentage of TH expression changes in the immunohistochemistry, as well as the p values of ANOVA between DPLs over time in the striatum are shown in Figure 1C. In these later periods, mainly at 60 DPL, we observed TH-positive perikarya in the injured striatum, when compared to the control side, which normally exhibits TH immunoreactivity exclusively in the neuropil. These cells were strongly stained for TH and its frequency was higher in sites close to the infusion of 6-OHDA (Figure 1B). Semi-quantitative analysis of the immunoblotting (Table 1) corroborates those found in immunohistochemistry.
In the SNpc a gradual and progressive decrease of TH immunoreactivity was observed in immunohistochemistry (Table 2, Figure 2A) and in immunoblotting (Table 1). The mean percentage of TH expression changes in the immunohistochemistry, as well as the p values of ANOVA between DPLs over time in the SNpc are shown in Figure 2B.
The CB1 analyses were performed only for immunohistochemistry, because a complex and distinct structure-related variation of its expression was observed and the immunoblotting analysis would not allow a detailed spatial resolution.
Our studies showed that CB1 receptor was present exclusively in neuropil in all structures of the basal ganglia analyzed. In the striatum, we found higher densities of CB1 in its dorsolateral portion. In the GP, CB1 was expressed throughout the structure, and in the SN, was restricted to the SNpr. The immunolabelling for CB1 was very specific, as we had no immunostaining in our negative controls, namely the omission of primary antibody and preadsorption of the primary antibody with the corresponding control peptide for CB1 (data not shown).
In the striatum, our data showed that there is no difference in the expression of CB1 in injured striatum in all DPL studied (Table 2 and Figure 6). However, in EGP the time course of CB1 expression showed a biphasic pattern, with an increase at short time points, which was gradually decreased at longer time ones (Table 2 and Figures 3 and 6). As for the EGP, the time course of CB1 expression in the IGP was biphasic, but with a different pattern. The increased expression of CB1 occurred only after 1 DPL, followed by a gradual decrease from 5 DPL (Table 2 and Figures 4 and 6). The SNpr exhibited a gradual decrease in CB1 immunoreactivity that seems to occur since the shorter time point (Table 2 and Figures 5 and 6).
Figure 6. Semi-quantitative analysis of CB1 staining in basal ganglia of PD-induced rats.
The quantification is represented by percentage in (A) striatum, (B) external globus pallidus (EGP), (C) internal globus pallidus (IGP) and (D) substantia nigra pars reticulata (SNpr) of rats submitted to unilateral intrastriatal injections of 6-OHDA after 1, 5, 10, 20, and 60 days post-lesion (DPL). Comparison between the percentage of experimental sides calculated from the control side to each group (dashed line). Statistical analysis by ANOVA (one way) with Tukey post-test. *p <0.05, **p<0.01 and *** p <0.001.
The CB1 expression data after the lesions are summarized in Table 3.
Table 3. Summary of CB1 expression changes in the basal ganglia.
↑↑ ↑ ↑ /↓ ↓ ↓ ↓ very large increase/decrease; (↑↑ ↑ /↓ ↓ ↓ large increase/decrease; (↑↑ /↓ ↓ moderate increase/decrease; (↑ /↓ little increase/decrease; (=) no change. All in relation to control side for each group.
The data above were generated by comparisons between experimental and control sides for each DPL. We have also performed another statistical comparison (ANOVA) between the experimental side/control side ratios for each DPL, to evaluate the differences over time. The mean percentage of CB1 expression changes in the immunohistochemistry, as well as the p values of ANOVA between DPLs over time in the striatum, EGP, IGP, and SNpr are shown in Figure 6.
As CB1 receptors are located in the axon terminals of GABAergic neurons in the basal ganglia , and Walsh et al.  described that the decrease of CB1 expression in SNpr could be an indirect toxic effect of 6-OHDA to GABAergic neurons, we have investigated the levels of GAD in the striatum and SN, and the immunolabeling for parvalbumin and calbindin in striatum (both immunolabeling known to be co-localized with GABAergic neurons in basal ganglia [34,35]), to verify a possible degeneration of these GABAergic neurons in the striatum caused by 6-OHDA. Semi-quantitative analysis of immunoblotting data showed no changes in GAD levels in the striatum and SN for all DPL studied (Table 1 and Figure S1). Our analysis showed no differences in the number of parvalbumin positive cells between the control and experimental striata (Table 2 and Figure S1).
Calbindin was observed mainly in cell body in the ventromedial portion. There was as an increase about 21% in the calbindin-positive cells for both 1 and 5 DPL (p<0.01 and p<0.001, respectively) (Table 2 and Figure S2).
Our results revealed a complex and distinct structure-specific variation of CB1 in the basal ganglia over time in 6-OHDA PD model. This variation was accompanied by an initial general TH reduction which is reversed by an increase at later periods in the striatum. No changes in the number of GABAergic neurons were observed in the striatum.
Several studies have shown the participation of the cannabinoid system in different neurodegenerative diseases and suggested its neuroprotective properties [21–23]. In this context, the high densities of CB1 receptors [1,8] and the endocannabinoid ligands found in the basal ganglia  have been explored in regard to PD, which has led to prospects for cannabinoid therapies.
There are few studies establishing a direct relationship between variation in the CB1 expression and the development of PD, as well as in animal models of PD. In addition, these studies, despite generating highly controversial data, are dedicated in most cases only to the striatum and/or SN [28,29,43].
Decreased levels of CB1 mRNA in the striatum were found in the PD model induced by reserpine in rats  and Walsh et al.  described the reduction of CB1 expression in the SN over time (1-28 days after lesion) in the 6-OHDA model. Since the main CB1 location in SNpr is in the GABAergic terminals, the authors attributed the decrease of CB1 expression to an indirect toxic effect of 6-OHDA to GABAergic neurons, which undergo degeneration and consequently decrease the CB1expression. However, we did not find any differences in GAD levels in the striatum and SN, neither decrease in the number of parvalbumin and calbindin positive cells in the striatum, at any time points studied, which led us to suppose that the CB1 decrease appears to be unrelated to a possible degeneration of GABAergic neurons. Indeed, in the case of calbindin we observed an increased expression in the striatum at shorter post-lesion periods, which could be related to its function as Ca2+ buffering. Studies show that in damaging processes there is an increase of Ca2+ levels, and the calbindin may increase the activity to buffering its overload, thus protecting neurons from excitotoxic damage [46,47].
The decreased levels of CB1 mRNA were also found in post-mortem brains of PD patients . A recent study employing a PET technique performed with specific CB1 radioligands reported a marked CB1 decrease in the SN of PD patients, concomitant with a slight increase of this receptor in dopaminergic projection areas .
A biphasic pattern of change in CB1 expression in the basal ganglia was observed in a previous study using mice with deletion of specific park genes [31,49]. In the early stages of asymptomatic PD (12 months of age) a desensitization/downregulation of CB1 occurs in GP and SN, particularly in the alpha-synuclein-deficient mice, which was associated to a dopaminergic dysfunction. In contrast, in later stages of PD (older than 12 months of age), characterized by a deep nigral degeneration associated to the appearance of parkinsonian symptoms, was related to a CB1 upregulation . The expression of CB1 in the GP seems to be influenced by degenerative processes that affect the basal ganglia, like Huntington's disease [50–52], and multiple sclerosis . Although explored in other neurodegenerative diseases, the CB1 expression in the GP is still not well studied in animal models of PD. Here we show for the first time the variation in the CB1 levels in all four basal ganglia structures that express CB1 in the PD 6-OHDA model, including both GP segments. This information is essential to understand the involvement of CB1 in the basal ganglia circuitry in the PD condition.
The literature points to the involvement of cannabinoid system in the basal ganglia circuitry and that this system is changed in neurodegenerative diseases [11,49]. It seems that the endocannabinoid and dopaminergic systems exert a mutual control on each other. In PD, for example, it has been suggested that changes in the cannabinoid system may participate in symptom generation or as part of a compensatory mechanism to counteract the unbalance in the physiology of the basal ganglia due to the lack of dopamine . Apart from the above-mentioned studies on the variations of CB1 expression, other studies showed changes in levels of endocannabinoids, such as anandamide  or changes in endocannabinoid membrane transporters and fatty acid amide hydrolase activity .
In relation to present data, the basal ganglia structure-specific time course variation in the CB1 expression could be a plastic response as part of a compensatory mechanism, as seen in studies of cannabinoid system in other pathways, such as retinal ablation , bilateral vestibular deafferentation , and in pilocarpine-induced epilepsy .
The data obtained here on CB1 changes may be related to GABA-dependent transmission into the basal ganglia. The decreased GABAergic transmission to SNpr and IGP promotes an increase in neuronal activity in both structures, whereas the increase in GABAergic transmission generates a larger inhibition in EGP . Under physiological conditions, the activation of pre-synaptic CB1 in GABAergic neurons inhibits the GABA release . Our hypothesis is that the decrease of CB1 in SNpr and IGP in the 6-OHDA PD model could be a plastic response as an attempt to increase the GABAergic transmission which was altered by the dopaminergic degeneration. Following the same reasoning, increased CB1 expression in the EGP may lead to a lower release of GABA, which could recover part of the neuronal activity (Figure 7).
Figure 7. Scheme of CB1 expression in basal ganglia of PD-induced rats.
Schematic representation of the CB1 receptors expression in the striatum, external globus pallidus (EGP), internal globus pallidus (IGP) and substantia nigra pars reticulata (SNpr). This scheme represents control side (A) and intrastriatal 6-OHDA injected side (B). Figure in A depicts the dopaminergic projection (full gray arrows) of the substantia nigra pars compact (SNpc) to the striatum, and GABAergic projections (full black arrows) of the striatum to EGP, IGP and SNpr, where CB1 receptors are found (gray squares). Figure in B represents the decreased dopaminergic (dotted gray arrows) and GABAergic (dotted black arrows) projections, the increased GABAergic projections (thicker full black arrows), increased CB1expression (bigger gray square), and the decreased CB1 expression (smaller gray square) after 6-OHDA injection. Our hypothesis is that the decrease of CB1 expression in the direct pathway (SNpr and IGP) could increase the GABAergic transmission, and the increase of CB1 expression in indirect pathway (EGP) could decrease the GABAergic transmission, which could together contribute to a restoration of normal thalamic activation. Both events may be a plastic response of the cannabinoid system due to the lack of dopamine.
Even for the EGP it is important to remember that despite the initial CB1 increase in shorter DPL, at 60 DPL there is a tendency to a decreased expression of CB1. Transient variations in the CB1 receptor expression has been observed by our group in different situations in the chick optic tectum, such as during embryonic development  and after retinal ablation . CB1 receptor variation seems to be common also in pilocarpine model of epilepsy, which exhibited a downregulation of hippocampal CB1 receptors in the acute phase, followed by compensatory upregulation and sprouting in the chronic phase of lobe temporal epilepsy . Similar pattern of hippocampal CB1 receptor change was seen in pilocarpine-induced status epilepticus . These data taken together suggest the involvement of changes in the CB1 expression in the neurodegenerative processes.
Finally, some authors describe that CB1 may increase local GABA levels in the EGP by reducing GABA reuptake from striatal afferents to that nucleus [13,60]. It is then possible that a decrease of CB1 in EGP at longer DPL is an attempt to decrease the release of GABA for this structure.
In conclusion, our results indicate a complex modulation of CB1 expression in the basal ganglia over time after intrastriatal injections of 6-OHDA, an animal toxin-induced PD model largely investigated. This modulation is in agreement with data from transgenic PD animal models and even more important, data from PD patients. The fact that changes in CB1 expression are structure-specific, led us to speculate that our data may help to explain the participation of the cannabinoid system in a possible compensatory mechanism in PD, possibly related to neuronal plasticity. Furthermore, our data appear to validate the intrastriatal injection of 6-OHDA as a good PD model to study the cannabinoid system in PD.
Temporal analysis of GAD levels in basal ganglia of PD-induced rats. Semi-quantitative analysis from immunoblotting. Mean ratio of GAD densitometry density data in relation to beta-actin, comparing the experimental with control side from each DPL. Statistic analysis by Paired Student t test.
Semi-quantitative analysis of calbindin and parvalbumin staining in basal ganglia of PD-induced rats. The quantification is represented by percentage in the striatum of rats submitted to unilateral intrastriatal injections of 6-OHDA after 1, 5, 10, 20 and 60 days post-lesion (DPL). (A) Parvalbumin (PV) and (B) Calbidin. Comparison between the percentage of experimental sides calculated from the control side to each group (dashed line). Statistical analysis by ANOVA (one way) with Tukey post-test. *p <0.05, **p<0.01 and *** p <0.001.
Thanks are also due to Adilson S. Alves for technical assistance.
Conceived and designed the experiments: GPCK CHYM CCR LRGB AST. Performed the experiments: GPCK CHYM CCR BMS. Analyzed the data: GPCK CHYM CCR BMS LRGB AST. Contributed reagents/materials/analysis tools: LRGB AST. Wrote the manuscript: GPCK CHYM CCR LRGB AST.
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Is the Subject Area "Cannabinoids" applicable to this article?
Is the Subject Area "Globus pallidus" applicable to this article?


Looking downright creepy, with the only movement visible as that of the wind, a few birds and the changing semaphores, this video by Menilmonde titled hypocentre, gives us a glimpse of what Paris devoid of human presence would look like.
Imagine an empty worrying Paris.
Imagine that human action is more harmful to our fragile planet.
First, "hypocentre" was a technical exercise for us. Then we decided to focus the film on the environmental side.
It's new for us, more specialists in the travel video, to try to do a short film.


Purcell Park is a 67 acre park located on Monument Avenue on the east side and on South Main Street on the south side of the park. There are two entrances to the park - one from Monument Avenue and the other from Miller Circle off of South Main Street. The park has three softball/baseball fields, four tennis courts, a playground, three picnic shelters, several restrooms, and a 1.5 mile walking trail. A large portion of the Bluestone Trail also runs through the park.


Merel Bechtold (born: February 27, 1992) is a Dutch guitarist, best known for her work with different symphonic metal bands such as Delain. She started playing guitar in 2007 at the age of fifteen. Half a year later she founded the band Purest of Pain, in which she plays lead guitar. Over the next two years, she began to play in larger, international events and festivals with bands like Suicide Silence, Unearth, MaYaN, Grave, All Shall Perish, Delain and others. In 2013, she released the single Momentum and in 2014 she starred at the large metal festival Wacken Open Air.
At the end of 2012, Bechtold performed her first performance with Delain. In 2013, for the first time, she filled in for Timo Somers, Delain's main guitarist. During the same period, she performed several concerts with the Purest of Pain group. In October 2014, she was contacted by Isaac Delahaye (Epica, ex-MaYaN) who had to leave MaYaN for other priorities. She played with them at two concerts in January 2015 as his replacement. At the second concert, the band asked her to become a permanent member.
In the summer of 2014, she became part of Anneke van Giersbergen's The Gentle Storm. She then played several concerts with Delain alongside Somers. In 2015, she again accompanied Delain at other concerts with Sabaton. From October 2015, Bechtold officially became a permanent member of Delain. In March 2018, Purest Of Pain's debut album "Solipsis" came finally out.


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Funding package targets research into production and integration of zero carbon hydrogen
Applications are being invited for a share of a £2mn funding package to research zero emission hydrogen production and integration.
On 2 September, the Engineering and Physical Sciences Research Council (EPSRC) set out how hydrogen and hydrogen-based, low-carbon liquid fuels will be key for the UK reaching net zero by 2050. With growing consensus of the role of deep decarbonisation of all sectors of the UK economy and the publication of the Hydrogen Strategy, the EPSRC is pledging to fund proposals that will develop solutions to advance zero emission hydrogen production and address challenges in integrating hydrogen into whole energy systems.
Areas of interest under the funding opportunity, which opened to applicants on 7 September, include research to address challenges associated with production routes such as electrochemical techniques, including electrolysis through renewables or nuclear energy; biological production routes; and solar-to-fuels routes to hydrogen. It will also consider cross-disciplinary projects that contain elements that contribute to the production or integration of zero emission hydrogen.
The deadline for applications is 4PM on 2 November 2021. Applications should have a full economic cost of up to £312,500, for which EPSRC will fund 80%.
The EPSRC is looking to fund up to eight projects, lasting for 18 months. Proposals funded through the opportunity will generate a platform of research and outcomes in key priority areas on which hydrogen research coordinators – funded through the hydrogen research coordinators opportunity – can then further developing in their respective centres, subject to future funding. This means successful projects through the zero emission hydrogen production and integration opportunity will be required to engage and work with hydrogen research coordinators in the development of their respective research programme plans and maximise the impact from both opportunities through sharing findings and dialogue.
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This is a chance to hear one of the greatest pieces in the classical music repertoire, Mozart's final piece he ever wrote, the Requiem.